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. 2022 Feb 8;8:56. doi: 10.1038/s41420-022-00837-5

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Comparison of proliferation and differentiation in control, rapamycin-treated, and MHY1485-treated ROs shown by immunostaining of Ki67 (yellow) and CHX10 (red) at 40 days of differentiation. In control and rapamycin-treated ROs, Ki67, and CHX10 expression was found in outer layers without any co-localization with HuC/D expression, while ROs with MHY1485 treatment showed upregulated expression of Ki67 and CHX10 throughout all RO layers, including RGC and outer neuroblastic cell layers. Disrupted retinal laminar structure was evident in MHY1485-treated ROs. B The average retinal thickness of in control, rapamycin-treated, and MHY1485-treated ROs. Arrowheads indicate co-localization of HuC/D and Ki67 expression. Data are expressed by mean ± S.E.M. *p < 0.05, **p < 0.01 by the Kruskal–Wallis test with post hoc analysis. Scale bar, 25 μm.